PMID- 30893423
OWN - NLM
STAT- MEDLINE
DCOM- 20200403
LR  - 20200403
IS  - 1460-2377 (Electronic)
IS  - 0953-8178 (Linking)
VI  - 31
IP  - 6
DP  - 2019 May 21
TI  - Tissue regulatory T cells and neural repair.
PG  - 361-369
LID - 10.1093/intimm/dxz031 [doi]
AB  - Inflammation and immune responses after tissue injury play pivotal roles in the 
      pathology, resolution of inflammation, tissue recovery, fibrosis and remodeling. 
      Regulatory T cells (Tregs) are the cells responsible for suppressing immune 
      responses and can be activated in secondary lymphatic tissues, where they 
      subsequently regulate effector T cell and dendritic cell activation. Recently, 
      Tregs that reside in non-lymphoid tissues, called tissue Tregs, have been shown 
      to exhibit tissue-specific functions that contribute to the maintenance of tissue 
      homeostasis and repair. Unlike other tissue Tregs, the role of Tregs in the brain 
      has not been well elucidated because the number of brain Tregs is very small 
      under normal conditions. However, we found that Tregs accumulate in the brain at 
      the chronic phase of ischemic brain injury and control astrogliosis through 
      secretion of a cytokine, amphiregulin (Areg). Brain Tregs resemble other tissue 
      Tregs in many ways but, unlike the other tissue Tregs, brain Tregs express 
      neural-cell-specific genes such as the serotonin receptor (Htr7) and respond to 
      serotonin. Administering serotonin or selective serotonin reuptake inhibitors 
      (SSRIs) in an experimental mouse model of stroke increases the number of brain 
      Tregs and ameliorates neurological symptoms. Knowledge of brain Tregs will 
      contribute to the understanding of various types of neuroinflammation.
CI  - (c) The Japanese Society for Immunology. 2019. All rights reserved. For 
      permissions, please e-mail: journals.permissions@oup.com.
FAU - Ito, Minako
AU  - Ito M
AD  - Department of Microbiology and Immunology, Keio University School of Medicine, 
      Shinjuku-ku, Tokyo, Japan.
FAU - Komai, Kyoko
AU  - Komai K
AD  - Department of Microbiology and Immunology, Keio University School of Medicine, 
      Shinjuku-ku, Tokyo, Japan.
FAU - Nakamura, Toshihiro
AU  - Nakamura T
AD  - Department of Microbiology and Immunology, Keio University School of Medicine, 
      Shinjuku-ku, Tokyo, Japan.
FAU - Srirat, Tanakorn
AU  - Srirat T
AD  - Department of Microbiology and Immunology, Keio University School of Medicine, 
      Shinjuku-ku, Tokyo, Japan.
FAU - Yoshimura, Akihiko
AU  - Yoshimura A
AD  - Department of Microbiology and Immunology, Keio University School of Medicine, 
      Shinjuku-ku, Tokyo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (Cytokines)
RN  - 0 (Receptors, Serotonin)
RN  - 0 (serotonin 7 receptor)
SB  - IM
MH  - Animals
MH  - Astrocytes/*immunology
MH  - Brain/*immunology
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Humans
MH  - Inflammation/*immunology
MH  - Mice
MH  - Receptors, Serotonin/metabolism
MH  - Reperfusion Injury/*immunology
MH  - T-Lymphocytes, Regulatory/*immunology
MH  - Wound Healing
OTO - NOTNLM
OT  - amphiregulin
OT  - astrogliosis
OT  - serotonin
OT  - stroke
OT  - tissue repair
EDAT- 2019/03/21 06:00
MHDA- 2020/04/04 06:00
CRDT- 2019/03/21 06:00
PHST- 2019/01/20 00:00 [received]
PHST- 2019/03/19 00:00 [accepted]
PHST- 2019/03/21 06:00 [pubmed]
PHST- 2020/04/04 06:00 [medline]
PHST- 2019/03/21 06:00 [entrez]
AID - 5410252 [pii]
AID - 10.1093/intimm/dxz031 [doi]
PST - ppublish
SO  - Int Immunol. 2019 May 21;31(6):361-369. doi: 10.1093/intimm/dxz031.